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      Increased Protein Carbonylation and Decreased Antioxidant Status in Anemic H. Pylori Infected Patients: Effect of Treatment

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          Abstract

          Background/Aim:

          Collective evidences suggest the causal association of Helicobacter pylori infection with iron deficiency anemia. Generation of free radicals against this bacterium can lead to turbulence in oxidative-antioxidative system. This study was undertaken to evaluate the marker of oxidative protein injury, protein carbonylation, and total antioxidant status in anemic H. pylori-infected patients and to observe the alteration in them after treatment for 1 month with oral ferrous sulfate and anti- H. pylori therapy. Twenty anemic H. pylori-infected patients were randomly divided into 2 groups. The H. pylori-infected patients in Group I received both iron supplementation and anti-H pylori therapy, whereas patients in Group II received only the iron supplementation. Fifteen healthy volunteers served as controls. All the study parameters were estimated after 1 month of the treatment.

          Materials and Methods:

          Protein carbonylation and total antioxidant status were estimated using colorimetric method. Hematologic parameters were evaluated using Sysmex-K-100 automated cell counter.

          Results:

          In anemic H. pylori-infected patients, the protein carbonyls (PCOs) were significantly increased, whereas the total antioxidant status, iron, hemoglobin, and ferritin levels were significantly decreased compared with the controls. In Group I, while the PCOs level decreased significantly, there was a significant increase in the total antioxidant status, iron, hemoglobin, and ferritin levels after 1 month. No significant alterations were noted in the levels of PCOs, total antioxidant status, iron, hemoglobin, or ferritin in Group II patients after 1 month of the treatment.

          Conclusions:

          The findings from this study indicate that treatment for both anemia and H. pylori infections is required for lowering the oxidative stress markers, which synergistically bring about an appropriate correction of anemia soon in these patients.

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          Most cited references27

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          Oxidation of biological systems: oxidative stress phenomena, antioxidants, redox reactions, and methods for their quantification.

          Reactive oxygen species (ROS) and other radicals are involved in a variety of biological phenomena, such as mutation, carcinogenesis, degenerative and other diseases, inflammation, aging, and development. ROS are well recognized for playing a dual role as deleterious and beneficial species. The objectives of this review are to describe oxidative stress phenomena, terminology, definitions, and basic chemical characteristics of the species involved; examine the biological targets susceptible to oxidation and the defense mechanisms of the organism against these reactive metabolites; and analyze methodologies, including immunohistochemical markers, used in toxicological pathology in the visualization of oxidative stress phenomena. Direct detection of ROS and other free radicals is difficult, because these molecules are short-lived and highly reactive in a nonspecific manner. Ongoing oxidative damage is, thus, generally analyzed by measurement of secondary products including derivatives of amino acids, nuclei acids, and lipid peroxidation. Attention has been focused on electrochemical methods based on voltammetry measurements for evaluating the total reducing power of biological fluids and tissues. This approach can function as a tool to assess the antioxidant-reducing profile of a biological site and follow changes in pathological situations. This review thus includes different topics essential for understanding oxidative stress phenomena and provides tools for those intending to conduct study and research in this field.
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            Protein oxidation in aging, disease, and oxidative stress.

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              DNA damage and oxygen radical toxicity.

              A major portion of the toxicity of hydrogen peroxide in Escherichia coli is attributed to DNA damage mediated by a Fenton reaction that generates active forms of hydroxyl radicals from hydrogen peroxide, DNA-bound iron, and a constant source of reducing equivalents. Kinetic peculiarities of DNA damage production by hydrogen peroxide in vivo can be reproduced by including DNA in an in vitro Fenton reaction system in which iron catalyzes the univalent reduction of hydrogen peroxide by the reduced form of nicotinamide adenine dinucleotide (NADH). To minimize the toxicity of oxygen radicals, the cell utilizes scavengers of these radicals and DNA repair enzymes. On the basis of observations with the model system, it is proposed that the cell may also decrease such toxicity by diminishing available NAD(P)H and by utilizing oxygen itself to scavenge active free radicals into superoxide, which is then destroyed by superoxide dismutase.
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                Author and article information

                Journal
                Saudi J Gastroenterol
                Saudi J Gastroenterol
                SJG
                Saudi Journal of Gastroenterology : Official Journal of the Saudi Gastroenterology Association
                Medknow Publications & Media Pvt Ltd (India )
                1319-3767
                1998-4049
                Jul-Aug 2012
                : 18
                : 4
                : 252-256
                Affiliations
                [1]Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
                [1 ]Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
                Author notes
                Address for correspondence: Dr. Bobby Zachariah, Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry - 605 006, India. E-mail: zacbobby@ 123456yahoo.com
                Article
                SJG-18-252
                10.4103/1319-3767.98430
                3409886
                22824768
                13ef31d0-4cce-44e9-9d8c-700e9649086b
                Copyright: © Saudi Journal of Gastroenterology

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 03 October 2011
                : 19 February 2012
                Categories
                Original Article

                Gastroenterology & Hepatology
                h. pylori,total antioxidant status,protein carbonyls,iron deficiency anemia

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